Aims/Introduction: Iron metabolism can directly or indirectly affect the occurrence and development of type 2 diabetes. This meta-analysis and systematic review aimed to analyze the association between serum iron metabolism indicators and type 2 diabetes. Materials and Methods: The databases PubMed and Embase were searched for studies on the correlations between serum iron metabolism indicators (iron, ferritin, transferrin, hepcidin and soluble transferrin receptor) and type 2 diabetes since January 2006. Relevant data were extracted from the included studies, and meta-analysis was carried out. Results: A total of 12 case-control and cohort studies were analyzed. Of the 12 studies, 11 described the correlation between serum ferritin levels and type 2 diabetes. The median and high serum ferritin concentrations were significantly associated with the risks of type 2 diabetes (odds ratio [OR] 1.20, 95% confidence interval [CI] 1.08-1.33 and OR 1.43, 95% CI 1.29-1.59, respectively). However, the low concentration was not correlated with the risk of type 2 diabetes (OR 0.99, 95% CI 0.89-1.11). No significant association was observed between serum soluble transferrin receptor and type 2 diabetes, whereas the soluble transferrin receptor-to-ferritin ratio was significantly inversely related to the risk of type 2 diabetes in the median and high ratio subgroups (OR 0.71, 95% CI 0.51, 0.99 and OR 0.65, 95% CI 0.45-0.95). Conclusions: The elevated serum ferritin was one of the risk factors for type 2 diabetes, and soluble transferrin receptor-to-ferritin ratio was inversely related to the risk of type 2 diabetes. A systematic review showed that serum transferrin and hepcidin might be directly or indirectly related to the development of diabetes.

Background: To assess the effect of obesity or a high body mass index (BMI) on the risk of severe outcomes in patients with coronavirus disease 2019 (COVID-19). Methods: Studies on the relationship between BMI or obesity and COVID-19 since December 2019. The odds ratio (OR) and weighted mean difference (WMD) with their 95% confidence intervals (CIs) were used to assess the effect size. Results: BMI was significantly increased in COVID-19 patients with severe illness (WMD: 1.18; 95% CI: 0.42–1.93), who were admitted to an intensive care unit (ICU) (WMD: 1.46; 95% CI: 0.96–1.97), who required invasive mechanical ventilation (IMV) (WMD: 2.70, 95% CI: 1.05–4.35) and who died (WMD: 0.91, 95% CI: 0.02–1.80). In Western countries, obesity (BMI of ≥30 kg/m 2 ) increased the risk of hospitalization (OR: 2.08; 95% CI: 1.22–3.54), admission to an ICU (OR: 1.54; 95% CI: 1.29–1.84), need for IMV (OR: 1.73, 95% CI: 1.38–2.17), and mortality (OR: 1.43; 95% CI: 1.17–1.74) of patients with COVID-19. In the Asian population, obesity (BMI of ≥28 kg/m 2 ) increased the risk of severe illness (OR: 3.14; 95% CI: 1.83–5.38). Compared with patients with COVID-19 and a BMI of <25 kg/m 2 , those with a BMI of 25–30 kg/m 2 and ≥30 kg/m 2 had a higher risk of need for IMV (OR: 2.19, 95% CI: 1.30–3.69 and OR: 3.04; 95% CI: 1.76–5.28, respectively). The risk of ICU admission in patients with COVID-19 and a BMI of ≥30 kg/m 2 was significantly higher than in those with a BMI of 25–30 kg/m 2 (OR: 1.49; 95% CI: 1.00–2.21). Conclusion: As BMI increased, the risks of hospitalization, ICU admission, and need for IMV increased, especially in COVID-19 patients with obesity. Ethics and dissemination: This systematic review and meta-analysis does not require an ethics approval as it does not collect any primary data from patients.

Background: S100 calcium-binding protein A16 (S100A16) is closely related to the onset and progression of tumors. Material/Methods: In the research, the mainly purpose was to investigate the effect of S100A16 on the proliferation ability, invasion, and angiogenesis of HeLa cells. An adenoviral vector overexpressing S100A16 (Ad-S100A16) was constructed and transfected into HeLa cells, forming a stable cells line of overexpression. The effect of S100A16 on the proliferative capacity of HeLa cells was evaluated by a Cell Counting Kit-8 (CCK-8) assay. Cell migration capacity was determined by a Transwell migration assay. Changes in matrix metalloproteinase-2 (MMP-2), MMP-9, E-cadherin, and vimentin expression were evaluated by a cell-based immunofluorescence assay. The effect of S100A16 on angiogenesis was verified by knockout experiment. Results: Overexpression of S100A16 significantly enhanced the proliferative and migratory capacities of HeLa cells (P<0.05), upregulated expression of matrix MMP-2, MMP-9, vimentin, phosphatidylinositol 3 kinase, and phosphorylated protein kinase B, and downregulated expression of E-cadherin. Vascular endothelial growth factor expression increased, phosphatase and tensin homolog expression decreased, and angiogenesis was positively correlated with S100A16 expression. These effects were largely mediated by the activation of the phosphatidylinositol 3 kinase/protein kinase B pathways. Conclusions: S100A16 could promote the proliferation, migration, and tumor angiogenesis of HeLa cells by regulating the phosphatidylinositol 3 kinase/protein kinase B signaling pathways.

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The aim of this meta-analysis was to assess the risks of endocrine adverse events in patients with malignancies treated with different types and different doses of immune checkpoint inhibitors (ICIs). PubMed and Embase were searched for randomized controlled trials on ICIs and endocrine adverse events since 2000, and meta-analysis was carried out. Twenty-six randomized controlled trials comprising 13 824 patients with malignancies were included. Compared with the other tumor therapies (used as a control group), patients treated with programmed death-1 inhibitors appeared to be at higher risks of hypothyroidism, hyperthyroidism, thyroiditis, hypophysitis or hypopituitarism, and type 1 diabetes mellitus, while there was no difference in the risk of primary adrenal insufficiency. It was also found that patients treated with cytotoxic T-lymphocyte-associated protein-4 inhibitors were at higher risk of hypophysitis or hypopituitarism, primary adrenal insufficiency, and hypothyroidism. In comparison, patients treated with programmed death-ligand 1 inhibitors were at higher risk of hyperthyroidism and hypothyroidism. Compared with the control group, both low-dose and high-dose ICI groups were at higher risk of hypothyroidism and hyperthyroidism, and the low-dose group had increased risk of thyroiditis and primary adrenal insufficiency. There was no significant difference in the risk of type 1 diabetes between the low-dose group and the high-dose group. The risk of hypophysitis or hypopituitarism in the high-dose group (relative risk, 20.12; 95% confidence interval, 8.02-50.46) was significantly higher than that in the low-dose group (relative risk, 4.92; 95% confidence interval, 2.11-11.47). The risk of endocrine adverse events was increased in patients treated with ICIs. Different types and doses of ICIs have varying characteristics of endocrine adverse events.

BackgroundOvarian cancer (OC) is the most lethal gynecological malignancy worldwide. Increasing evidence indicates that TBC domain family is implicated in various cellular events contributing to initiation and development of different cancers, including OC. However, the role of TBC1D2, a crucial member of TBC domain family, remains unclear in OC.MethodsIHC and qRT-PCR were employed to determine TBC1D2 expression in OC tissues and cells. In vitro and in vivo assays involving proliferation, migration, invasion were performed to explore the role of TBC1D2 in OC development. The underlying mechanism by which TBC1D2 promotes OC metastasis were elucidated using bioinformatics analysis, western blotting and co-immunoprecipitation.ResultsUpregulation of TBC1D2 was found in OC and was associated with a poor prognosis. Meanwhile, TBC1D2 promoted OC cell proliferation, migration, and invasion in vitro and facilitated tumor growth and metastasis in vivo. Moreover, TBC1D2 contributed to OC cell invasion by E-cadherin degradation via disassembling Rac1-IQGAP1 complex. In addition, miR-373-3p was screened out and identified to inhibit OVCAR3 invasion via negative regulation of TBC1D2.ConclusionOur findings indicated that TBC1D2 is overexpressed in OC and contributes to tumor metastasis via E-cadherin degradation. This study suggests that TBC1D2 may be an underlying therapeutic target for OC.

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